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Oncostatin M is a secreted niche factor responsible for quiescence induction
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data revealed that OSM alleviated postinfarction cardiac remodeling and dysfunction by enhancing cardiomyocyte autophagy. OSM holds promise as a therapeutic target in treating HF after MI through Obeta receptor by inhibiting Mst1 phosphorylation.
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TRAF5 is crucially involved in OSM-mediated lung inflammation probably by inducing lung stromal/fibroblast cell activation.
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OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 and IL-21; it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3, and STAT5; observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3, and STAT5
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In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacological blockade of OSM significantly attenuates colitis.
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these results support the proinflammatory role of OSM when it is overexpressed in the skin. However, OSM expression was not required in the murine model of psoriasis induced by topical application of imiquimod, as demonstrated by the inflammatory phenotype of OSM-deficient mice or wild-type mice treated with anti-OSM antibodies.
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OSM (mOSM) signals mainly via an OSM receptor (OSMR)-gp130 heterodimer and binds with only very low affinity to mLIFR.
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Loss of Oncostatin M Signaling in Adipocytes Induces Insulin Resistance and Adipose Tissue Inflammation in Vivo.
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mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf/Mek/Erk signaling pathway through the OSM receptor Obeta
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Oncostatin M and interleukin-31: Cytokines, receptors, signal transduction and physiology.
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OSM plays multiple critical roles in the maintenance and development of the hematopoietic microenvironment in the bone marrow at a steady state as well as after injury.
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OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF and bFGF in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI.
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The mechanism of Oncostatin M on cardiac ischemia/reperfusion injury is partly mediated by the Notch3/Akt pathway.
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OSM-induced osteogenesis and upregulation of osteogenic gene products require activity of PKCdelta.
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The Notch signaling pathway was found to be one of the signaling pathways that inhibit OSM-induced MC3T3-E1 cell proliferation and differentiation.
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administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation
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A novel role for OSM during pneumonia as an important signal to epithelial cells for chemokine induction mediating neutrophil recruitment.
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These results suggest that mOSM, a product of macrophages, sustains intramembranous bone formation by signaling through Osmr and Stat3, acting on the recruitment, proliferation, and/or osteoblast differentiation of endosteal mesenchymal progenitor cells.
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In astrocytes but not microglia, phosphorylation of STAT1 and STAT3 occurred in response to OSM, whereas both microglia and astrocytes responded to hyper-IL-6 (IL-6 linked to the soluble IL-6 receptor).
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Following spinal cord injury, OSM is produced at the lesion site, where it protects the CNS from further damage and promotes recovery
